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From Herlev University Hospital, Copenhagen University Hospital, and Bispebjerg University Hospital, Copenhagen, Denmark.

Grant Support: By the Danish Heart Foundation, the Danish Medical Research Council, University of Copenhagen, the European Organization for the Control of Circulatory Diseases, the Beckett Fund, Manufacturer Frands Køhler Nielsen and Wife's Grant, and King Christian the Xth Fund.

Acknowledgment: The authors thank Marianne Lodahl for technical assistance and the participants of the Copenhagen City Heart Study for their willingness to participate.

Angiotensinogen is a key protein in the renin–angiotensin system, which influences vascular tone, renal sodium reabsorption, and blood pressure (1). Huge scientific interest was generated when one of two amino acid–changing mutations in the angiotensinogen gene, M235T but not T174M, was found to be associated with elevated plasma angiotensinogen levels (2), elevated blood pressure (2), ischemic heart disease (3), and ischemic cerebrovascular disease (4). The M235T mutation changes a nonpolar amino acid to a polar amino acid and thus potentially changes the tertiary structure of the protein. Because of this, it is likely that such a mutation may also influence protein function.

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Figures

Study design.

First, Copenhagen City Heart Study controls were compared with patients who had ischemic heart disease, myocardial infarction, or ischemic cerebrovascular disease (case–control studies 2a, 2b, and 2c), ascertained through hospital referrals to the same hospital where the Copenhagen City Heart Study was performed. Second, persons in the Copenhagen City Heart Study who had ischemic heart disease, myocardial infarction, or ischemic cerebrovascular disease (case–control studies 1a, 1b, and 1c) were compared with Copenhagen City Heart Study controls.

Risk for ischemic cerebrovascular disease in women and men according to angiotensinogen genotype.

Odds ratios and 95% CIs were calculated as a function of M235T, T174M, and M235T/T174M genotypes by using logistic regression analysis in three ways: 1) adjusted for age; 2) adjusted for age, body mass index, diabetes mellitus, smoking, hypertension, total cholesterol level, high-density lipoprotein cholesterol level, triglyceride level, and, in women, menopausal status; and 3) matched for age, smoking, hypertension, and cholesterol levels. Double slashes indicate a break in the odds ratio axis. *Numbers of persons in each genotype subgroup are from the age-adjusted analysis; these numbers were lower in multifactorial-adjusted and matched analyses. †No odds ratio could be calculated because no case-patients were included in this genotype subgroup.

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Summary for Patients

The summary below is from the full report titled “Angiotensinogen Mutations and Risk for Ischemic Heart Disease, Myocardial Infarction, and Ischemic Cerebrovascular Disease. Six Case–Control Studies from the Copenhagen City Heart Study.” It is in the 15 May 2001 issue of Annals of Internal Medicine (volume 134, pages 941-954). The authors are AA Sethi, A Tybjærg-Hansen, MLM Grønholdt, R Steffensen, P Schnohr, and BG Nordestgaard.

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